Mineralocorticoid activity of 19-nor-DOC and 19-OH-DOC in toad bladder.
Adrenal enucleation is followed by a period of increased sodium reabsorption thought to be due to excess mineralocorticoid activity. However, it has not been demonstrated that increased production of any known mineralocorticoid accounts for this antinatriuresis. Recently, 19-hydroxydeoxycorticosterone (19-OH-DOC) was found in incubates of regenerating adrenal capsules 3-4 days postenucleation and 19-nordeoxycorticosterone (19-nor-DOC) was identified in the urine of rats with regenerating adrenals. Because it was possible that these hormones might play a role in the sodium retention after adrenal enucleation, we compared the mineralocorticoid activity of these steroids to aldosterone using the toad bladder. Using short-circuit current as a measure of sodium transport, we found that 19-OH-DOC (10(-8) M) had no significant effect on sodium transport. However, 19-nor-DOC (10(-8) M) increased sodium transport to a degree not different from aldosterone (10(-8) M). Furthermore, the onset of action, duration of activity, and inhibition of effect of 19-nor-DOC by spironolactone were not different from that of aldosterone. We conclude that 19-nor-DOC exhibits a significant effect on sodium transport and thus has the potential to play a role in the sodium retention following adrenal enucleation. Under the conditions of these studies, 19-OH-DOC exhibited no effect on sodium transport.
D000450:Aldosterone / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002024:Bufo marinus; D003900:Desoxycorticosterone / Q000031:analogs & derivatives* / Q000494:pharmacology; D007700:Kinetics; D012964:Sodium / Q000378:metabolism*; D013148:Spironolactone / Q000494:pharmacology; D001743:Urinary Bladder / Q000502:physiology*
C027855:19-hydroxydeoxycorticosterone; D013148:Spironolactone; D003900:Desoxycorticosterone; C019026:19-nordeoxycorticosterone; D000450:Aldosterone; D012964:Sodium